SFT: On Genetic Entropy

Sure, bacteria are 10^-9 to 10^-7 versus 10^-6 to 10^-4 for RNA viruses. A nice 10^3 between top and bottom ranges. Which is coincidentally the same difference as their effective population sizes…

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Please refer back to my previous comment:

I have no evidence for the fitness distribution of nearly neutral mutations, and neither do you. That was my point. Count me as among those who think you don’t understand much of what you quote.

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Did you ever bother to look at the difference between mutation rates of RNA viruses vs bacteria? If not, I invite you to do so, the result may come as a surprise to you.

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Absolute fitness sounds « Platonic »! Absolutely!
This is what Maynard Olson argues about the human genome in his Science letter below.
https://science.sciencemag.org/content/331/6019/872.3.full

People might be interested in this new preprint from the Thornton lab, which is relevant to gpuccio’s analysis discussed earlier:

The final paragraph:

Finally, our observations suggest that the sequence-structure-function associations apparent in sequence alignments are, to a significant degree, the result of shared but contingent constraints that were produced by chance events during history (Gong et al., 2013; Harms and Thornton, 2014; Starr et al., 2018; Starr et al., 2017). Present-day proteins are physical anecdotes of a particular history: they reflect the interaction of accumulated chance events during descent from common ancestors with necessity imposed by physics, chemistry and natural selection. Apparent “design principles” in extant or evolved proteins express not how things must be—or even how they would be best—but rather the contingent legacy of the constraints and opportunities that those molecules just happen to have inherited.

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Hmmm. I recall some-one writing this:

“And if you peruse the comments here, you’ll see a pattern (the same pattern I found previously): no one is willing to address the actual arguments. Instead they want to create smokescreens and fake “analogies” that have nothing to do with the premises of my argument.”

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Did you ever bother to read my response to Paul on this exact question? If not, I invite you to do so, the result may come as a surprise to you.
Hint: It was posted 3h before your comment.

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They’re also much simpler than both bacteria and “higher organisms”. You yourself have said that according to this GE idea, simpler organisms should be more resistant to GE. But you don’t have a measurement of their degree of simplicity, nor do you know how this supposed GE correlates, in magnitude, with the degree of simplicity. Holding other measures constant, how does a 1%, or 5%, or 90% drop in simplicity affect the rate of GE? Since you clearly have no idea, you can’t at all claim that it should be different for bacteria or viruses than for “higher organisms”.

Simply put, you don’t have an equation that suggests what the rate of fitness decline should be, where the degree of “simplicity” of the organism is a factor in the equation.

You just have assertions, no evidence for the supposed extreme prevalence of invisibly deleterious mutations, and in fact only evidence against. In fact the lack of evidence for your case is so overwhelmingly, and in fact so much against it, that you’re now saying that some of the people advancing the GE disagree on whether it even happens to “simple” organisms like bacteria, which is largely the type of organism from which the DFE of mutations are measured in.

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Evolution is not capable of taking "a single cell" and developing it into a human being. Either you don’t understand evolution, you’re mixing it up with maturation, or you’re being deliberately deceptive.

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Better yet, can he just give the relevant equation that has organismal simplicity as a term? Because it would seem that the DFE and effective population size determine if it happens, while mutation rate only determines how fast it happens if it happens at all.

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Just wondering. Would this thread benefit from focussing in on just one problem at a time with fewer inputs?
As a relatively new person to the board, trying to follow this thread is like trying to follow each ball on the break of a pool game. Too many things flying around and no real chance to focus on the details of any one thing.

Sorry if not my place to butt in here, I am not trying to be a moderator. I am finding it interesting but hard to keep up.

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You might note that I am a population geneticist, or at least I play one in the scientific literature. It’s probably true that no mutation has precisely zero effect on fitness. Nonetheless, lots and lots of mutations – the great majority of mutations in humans – have such a small effect that they have zero practical consequences.

No, you’re not. Real biology looks at evidence from real organisms, based on observation and experiment. I study biology – that’s why I keep asking you for evidence to support your claims. What you’re providing me are analogies and quotations from authorities. Those are effective in literature and theology, not in biology.

You really do not seem to understand the situation here, or the essential reason that biologists (the ones who study real biology) don’t think there’s anything to Sanford’s claims. In a YEC world, all organisms start with perfect genomes. In that world, most mutations are indeed very slightly deleterious because (in your terms), we’re starting with perfectly designed machines and every change is for the worse. In an evolutionary world, in which all genomes are the result of mutation and selection, no genome was ever perfect. They’re not perfect machines. They’re Fords from the 1960s: poorly engineered, with lots of things that could be done better, but quite capable of functioning. In that world, most effectively neutral mutations aren’t damaging a perfect machine – they’re making insignificant differences to a machine that has always been imperfect. Every time you say something like ‘it’e much easier to damage a machine than improve it’ as though that settled the question, you demonstrate that you don’t understand what the question even is.

Our base expectation is that genetic entropy should widespread if YEC is correct and should not be occurring if mainstream science is correct. That being the case, if you want to argue against evolution, you have to show that genetic entropy is actually a ubiquitous feature of real biology. And that means you have to show either (1) that the fitness of most organisms is declining, or (2) that mutations of tiny effect are overwhelmingly deleterious. Since you can’t provide evidence that either of these is true, the entire GE argument is pointless. (Indeed, since (1) is clearly false, it provides evidence that YEC isn’t true.)

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In principle, absolutely. In practice, that’s difficult since everyone thinks their own ideas are important. Plus, lots of people like hearing themselves talk. Me, I think it would be best to focus on the core idea of genetic entropy and how it does or doesn’t relate to real biology. But that’s because that’s the line I want to push.

Agreed it is difficult. I would just be more interesting for uninformed observers like me to see a topic pursued and debated without ever finishing a point and bouncing between contributors. Also, seems like we have only one or two people defending the entropy thesis while getting piled on by lots of people and thoughts, however valid they all may be

Not too sure how a forum could cater for my naive optimism :grinning:

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In other words, you are reserving the right to ignore what is said in the published literature any time you don’t want to acknowledge it.

Are they really effective in literature and theology? I suspect not.

Well, analogies and their kin – metonymies, synecdoches, similes, and the whole rhetorical stable – are indeed effective literary tools. A great deal of theology is based on interpreting authoritative spiritual texts, but whether that’s effective or not is in the eye of the observer (which I believe is a synecdoche).

Great! You hadn’t mentioned that previously, so I didn’t know. I guess I am not in the know enough to draw that conclusion from your title of ‘computational biologist’.

Then you agree with Dr. Sanford on this point. But please don’t play dumb: everything we know about mutations, both from theory and from practice, shows they are overwhelmingly damaging. That means that your above statement is very revealing, because you just admitted that the vast majority of mutations are not selectable. The usual story (just as told by Darwin himself) is that we can account for the greatness of our own biological design by the subtle working of natural selection over eons. But the truth is uglier: most of what’s going on is drift…in other words, the completely unguided piling on of haphazard accidental changes.

You’re trying to use a version of the ‘god of the gaps’ argument, but in this case it’s ‘beneficial mutations of the gaps’. You know it, I know it.

Real biology looks at evidence from real organisms, based on observation and experiment.

Real biology offers next to no support for the idea of beneficial mutations, and overwhelming evidence of damaging mutations leading to genetic disease. You are retreating into the unknown. You are ignoring the way information works on a fundamental level, and you are not applying what we know about information to the genome. The genome is not about chemistry or physics: it’s about information.

You really do not seem to understand the situation here, or the essential reason that biologists (the ones who study real biology) don’t think there’s anything to Sanford’s claims.

Give me a citation for this claim, specifically with regard to Sanford. Sanford himself happens to be a biologist who studies real biology. He’s a pioneer in genetic engineering.

The population geneticists I’ve been quoting for you must be YECs, then, because they have confirmed that the general principle that “it’s much easier to break a machine than to improve upon it” does apply to mutations generally speaking (which would include our effectively neutral ones).

A machine need not be perfect for this principle to apply. If you make a whole lot of very tiny, haphazard changes to a 1960’s Ford, I can promise you it will not evolve into a Tesla. Want to try this out? Engineering is always more difficult than breaking things, and that applies whether you start out with a perfect machine or merely a functional machine.

I’m in good company, since I’ve been quoting that statement from the population genetics literature itself, with regards to mutations. You are deliberately ignoring its application here.

That’s incorrect. Case studies are difficult because of the timescale involved, but one such study has been completed by Carter and Sanford themselves, and published.

I’m sorry, but stating the truth is not playing dumb. Everything we know about mutations, and we know quite a lot, tells us that (for example) in ~90% of the human genome the precise sequence doesn’t matter at all. There may be tiny efficiency differences to some sequence configurations, but they’re negligible; if you changed every base in that part of the genome, you’d still have a perfectly functional human that was indistinguishable from others. Sanford is simply wrong.

Stripping away the tendentious language: yes, the neutral theory of evolution is largely correct, and most genetic variation and change in organisms like humans is selectively neutral and almost all of it is unimportant for biology. This is a standard part of evolutionary theory.

Just an observation that may help you in the future: as far as I can tell, every time you say something like ‘You know, I know it’, you’re wrong.

This is a tangent from the current discussion, but it’s also wrong – utterly, even hilariously wrong, Seriously, do you have any idea how ridiculous it is telling someone who’s spent decades studying beneficial mutations that they don’t exist?

I’ve deleted most of the rest, since it’s nothing but a continued repetition of your claims, still without any evidence to support them. Except for this:

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